The noncoding RNA CcnA modulates the master cell cycle regulators CtrA and GcrA in Caulobacter crescentus

PLoS Biol. 2022 Feb 22;20(2):e3001528. doi: 10.1371/journal.pbio.3001528. eCollection 2022 Feb.

Abstract

Bacteria are powerful models for understanding how cells divide and accomplish global regulatory programs. In Caulobacter crescentus, a cascade of essential master regulators supervises the correct and sequential activation of DNA replication, cell division, and development of different cell types. Among them, the response regulator CtrA plays a crucial role coordinating all those functions. Here, for the first time, we describe the role of a novel factor named CcnA (cell cycle noncoding RNA A), a cell cycle-regulated noncoding RNA (ncRNA) located at the origin of replication, presumably activated by CtrA, and responsible for the accumulation of CtrA itself. In addition, CcnA may be also involved in the inhibition of translation of the S-phase regulator, GcrA, by interacting with its 5' untranslated region (5' UTR). Performing in vitro experiments and mutagenesis, we propose a mechanism of action of CcnA based on liberation (ctrA) or sequestration (gcrA) of their ribosome-binding site (RBS). Finally, its role may be conserved in other alphaproteobacterial species, such as Sinorhizobium meliloti, representing indeed a potentially conserved process modulating cell cycle in Caulobacterales and Rhizobiales.

Publication types

  • Research Support, Non-U.S. Gov't

MeSH terms

  • Bacterial Proteins / genetics
  • Bacterial Proteins / metabolism
  • Caulobacter crescentus* / genetics
  • Caulobacter crescentus* / metabolism
  • Cell Cycle / genetics
  • DNA-Binding Proteins / metabolism
  • Gene Expression Regulation, Bacterial / genetics
  • Promoter Regions, Genetic
  • RNA, Untranslated / genetics
  • Transcription Factors / metabolism

Substances

  • Bacterial Proteins
  • DNA-Binding Proteins
  • RNA, Untranslated
  • Transcription Factors

Associated data

  • Dryad/10.5061/dryad.4mw6m909k

Grants and funding

This research was funded by the Agence Nationale Recherche (ANR; ANR-17-CE20-0011-01) to EGB. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.